A p53-derived apoptotic peptide derepresses p73 to cause tumor regression in vivo
J. Clin. Invest. Helen S. Bell, et al. 117:1008 doi:10.1172/JCI28920 [Go to this article.]

Figure 4
Expression of iASPP or interference with p73 inhibits 37AA-mediated cell death. (A) Saos-2 cells were transfected with the indicated plasmids and then infected with an adenovirus (Ad) expressing ΔN-p73α or empty virus control (Con). After 48 hours, cells were analyzed for cell death by flow cytometry or for expression of transfected plasmids by Western blotting. (B) Saos-2 cells that had been infected with a retrovirus expressing either an shRNA directed against TA-p73 (pRS-p73) or a scrambled control (pRS-Scr) were transfected with the indicated plasmids. After 48 hours, cells were analyzed for cell death by flow cytometry or for expression of transfected plasmids by Western blotting. (C) Saos-2 cells were transiently cotransfected with the indicated amounts of 37AA and iASPP. After 48 hours, cells were analyzed for cell death by flow cytometry and for expression of transfected plasmids by Western blotting. (D) The effects of iASPP knockdown by RNA interference in p53-null cells were determined. Saos-2 cells were transfected with plasmids expressing 2 different shRNAs that target iASPP or a scrambled shRNA control. The effects of the shRNAs on transfected iASPP expression were determined by Western blotting after 24 hours, and the effects on long-term survival were determined by assessing the clonogenic capacity of the cells. G418 con, control for drug activity; cells were mock-transfected and selected with G418. Original magnification, ×1.